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Biomedical subjects

B Renault

Publications and source records attributed to B Renault.

At least 55 records · Page 3Linked to original sources
PubMed1996

Microsatellite instability and mutations of p53 and TGF-beta RII genes in gastric cancer.

To investigate the molecular mechanism of gastric carcinogenesis, we analyzed genetic instability and p53 gene mutations in 40 primary gastric carcinomas. Tumor samples were from untreated patients with no family history suggestive of genetic predisposition to cancer. We screened six microsatellite loci by the polymerase chain reaction (PCR) method, and exons 5-8 of the p53 gene by the PCR-based denaturing gradient gel electrophoresis and sequencing techniques. Microsatellite instability was detected in 32.5% (13/40), and gene mutations in 40% (16/40), of the tumors analyzed. No statistically significant associations were found between genetic alterations and clinico-pathological variables (with the exception of diffusion of lymph node metastases, which was inversely associated with the presence of microsatellite alterations; P < 0.01). Interestingly, a negative association was found between genetic instability and p53 gene mutations: 11 out of 13 tumors showing instability proved to carry a nonmutated p53 gene versus 2/13 carrying a mutated gene (P = 0.03). These observations suggest that genetic instability and p53 gene mutations play a crucial role in the gastric carcinogenic process, but likely act through distinct pathways during cancer development. However, genetic instability is not in and of itself neoplastic. Therefore, we investigated whether insertion/deletion mutations of the polyadenine tract within the transforming growth factor-beta type II receptor gene (TGF-beta RII) were frequently present in gastric tumors with an RER+ (replication error) phenotype. We found RII mutations in 8/40 (20%) samples: mutations were present in 7/13 (54%) RER+ tumors versus 1/27 (4%) RER- cases (P < 0.001).

DNA Mutational Analysis↗
PubMed1996

Brain events related to normal and moderately scrambled faces.

The neural basis of normal and scrambled face processing was investigated by recording evoked potentials from 21 electrodes at standard EEG sites, with respect to a nose reference. Temporal negativities were found that result from two overlapping phenomena: they arise from the polarity reversal on temporal electrodes of the vertex P2, a positive wave peaking about 170-200 ms after the onset of a face stimulus, and also from an overlapping 'processing negativity' of long duration associated with the processing difficulty of the scrambled face stimulus. The comparisons of scalp potential and current density mappings support the proposal that some neuronal networks are active both for faces and scrambled faces and are compatible with the involvement of the superior temporal sulcus, the inferotemporal cortex and the parahippocampal and fusiform gyri, whereas the processing negativity would only involve the deepest generators of this network. Furthermore, the encoding of both faces and scrambled faces seems to take place predominantly in the right hemisphere.

Adult↗
PubMed1996

[Bowel complications in gynecologic laparoscopic surgery and their immediate repair without laparotomy. Four cases].

Laparoscopic surgical procedures are increasing throughout the world, and with this increase in its utilization, a renewed interest in its possible complications. We presented four case reports of bowels injuries and their repair by laparoscopy. We reviewed the literature and discuss common complications with suggestions to avoid such injuries and for management. We conclude that small and large bowel enterostomies can be repaired safely via the laparoscope with minimum morbidity in patients with a prepared bowel. More serious complications occur if visceral trauma is not handled immediately. There is no place for adopting a "wait and see" approach.

Adult↗
PubMed1996

N400-like potentials elicited by faces and knowledge inhibition.

Within the theoretical framework of reference, the brain errs in processing complex stimuli, such as faces. Thus, these stimuli not only activate accurate representations but also inaccurate representations corresponding to known persons who resemble the face stimulus, and hence knowledge about these known persons. Since more errors are made in processing unfamiliar than familiar stimuli, these inaccurate activations are assumed to be more frequent, and/or more intense, with unknown than with known faces. Moreover, top-down mechanisms favor representations of stimuli that are congruent with the context, and representations of known persons, even if inaccurate, receive an additional amount of activation in contexts wherein known faces are expected. Inaccurate representations have to be inhibited to achieve accurate recognition. Thus, more inhibition would be required for unknown than for known faces, and in contexts wherein known faces are expected. The aim of the present work is to study the hypothesis that the N400 component of the event-related potentials (ERPs) reflects the inhibition of knowledge, and to see whether this hypothesis accounts for the N400-like potential elicited by faces. To achieve that goal, ERPs to known and unknown faces were recorded while the richness in known faces of each experimental block, and thus the expectancy for known faces, was manipulated. Consistent with the hypothesis, the amplitudes of the N400-like components were greater in conditions where more inhibition was required, i.e. for unknown rather than for known faces, and in the context of the block rich in known faces. This context effect was larger for unknown than for faces, and in the context of the block rich in known faces. This context effect was larger for unknown than for known faces.

Adult↗
PubMed1995

Localization of the human achaete-scute homolog gene (ASCL1) distal to phenylalanine hydroxylase (PAH) and proximal to tumor rejection antigen (TRA1) on chromosome 12q22-q23.

ASCL1, the human achaete-scute homolog, is a helix-loop-helix transcription factor that was previously assigned to chromosome 12 using a rodent-human somatic hybrid panel. We now placed this gene on a yeast artificial chromosome contig encompassing position 119 cM of the Généthon genetic map between the two genes phenylalanine hydroxylase (PAH) and tumor rejection antigen 1 (TRA1). We also localized ASCL1 in the 12q22-q23 cytogenetic interval by using fluorescence in situ hybridization.

Antigens, Neoplasm↗
PubMed1995

A second-generation YAC contig map of human chromosome 12.

Human chromosome 12 constitutes approximately 4.5% of the human genome and has an estimated size of 135 million base pairs (Mb). We have started to construct a high-resolution physical map of chromosome 12 as overlapping yeast artificial chromosomes (YACs), using as a foundation the first-generation physical map of this chromosome covers nearly 102 Mb of DNA and includes 426 highly polymorphic, monomorphic and gene-based markers. We also mapped 119 of the YACs, most of which are part of the physical map, by cytogenetic methods. Thus the map integrates genetic, physical and cytogenetic data and provides information about the organization of this chromosome and will help in the localization and cloning of disease-related genes. The strategy used here to generate the chromosome-12 map could be applied for the rapid construction of physical and expression maps for other human chromosomes.

Base Sequence↗
PubMed1995

A comparative study of ERP correlates of psychometric and Piagetian intelligence measures in normal and hyperactive children.

Verbal and performance scores of the Wechsler Intelligence Scale for Children-Revised (WISC-R 1981) and of a Piagetian battery, the Cognitive Development Scale for Children (EDC 1984), were obtained on 30 normal control and 19 hyperactive 6-8-year-old children. Amplitudes and latencies of a fronto-central P250 and of the parieto-occipital N250, P350 and P500 were measured concurrently in 4 categorization tasks derived from tests of the WISC-R and EDC batteries. Spearman correlations were computed between the intelligence and the ERP factor scores. Results showed that age-related and age-corrected Wechsler's scores were correlated with similar ERP changes (reduced amplitude, decreased latency). With regard to the amplitude changes, each type of intelligence was associated with a specific ERP pattern. The verbal scores were correlated with the P350 and the P500 amplitudes, and the performance scores with the frontal P250 and occipital N250 amplitudes. By contrast, Piagetian development and intelligence scores yielded ERP correlates in the opposite direction: P500 amplitude was negatively correlated with raw EDC scores, but positively with scaled EDC scores. In addition, Piagetian intelligence was not related to the general peak latency decrease with age. In hyperactive children, additional negative correlations were found between P250 amplitude and the subjects' verbal test scores. Correlations with some performance tests that were negative in normal controls, were positive in hyperactive children. In addition, latency-based correlations found in normal controls were lacking in hyperactive children. These findings provide strong evidence that intelligence comprises different components related to different subsets of cognitive processes, as indexed by different ERP waves. They also suggest that the development and intelligence do not always rely on the same changes, and that intelligence forms may not be referred to the same use of the same processes in hyperactive and normal children.

Attention Deficit Disorder with Hyperactivity↗
PubMed1994

A targeted chain-termination mutation in the mouse Apc gene results in multiple intestinal tumors.

Germ-line mutations in the human adenomatous polyposis coli (APC) gene result in familial adenomatous polyposis, an autosomal dominant disorder characterized by the early onset of multiple adenomatous polyps in the large bowel with a high likelihood of developing colorectal carcinomas. To understand the role of APC in intestinal tumor formation, we have introduced a chain-termination mutation in the 15th exon of the mouse Apc gene and employed it to modify the endogenous gene by homologous recombination in embryonic stem cells. Mice which are heterozygous for the Apc gene modification progressively develop intestinal tumors in a manner that is similar to that observed in patients with familial adenomatous polyposis and in mice which carry a mutation called multiple intestinal neoplasia (Min). Our results indicate that the Apc gene modification is a critical event in the initiation of intestinal tumor formation and results in an autosomal dominant predisposition toward development of spontaneous colonic and intestinal tumors in mice.

Adenomatous Polyposis Coli↗
PubMed1994

K-ras and p53 gene mutations in pancreatic cancer: ductal and nonductal tumors progress through different genetic lesions.

We studied K-ras and p53 gene mutations in a panel of 57 primary pancreatic cancers including ductal and nonductal tumors. DNAs were obtained from formalin-fixed, paraffin-embedded material. Target sequences were amplified by polymerase chain reaction and analyzed by denaturing gradient gel electrophoresis and sequencing. Both K-ras and p53 genes were frequently mutated in ductal cancers (25 of 35, 71.4%; 18 of 35, 51.4%, respectively). K-ras mutations were confined to the second position of codon 12 where base transitions and transversions were equally observed. p53 changes were mainly missense mutations. Transitions and transversions were found equally with a prevalence of G:C-->A:T changes among transitions. No gene alterations were present in the 6 exocrine nonductal tumors and (with one exception) in the 12 endocrine tumors analyzed. Our results indicate that mutated K-ras and p53 genes can cooperate in the establishment of ductal pancreatic cancers, whereas other genetic events have to be present in nonductal tumors. Moreover, K-ras alterations may represent an early event in ductal tumorigenesis, as suggested both by the high gene mutation frequency and by the presence of mutations in low-grade tumors. On the contrary, p53 gene changes seem to represent an event required for the malignancy progression of ductal tumors from lower to higher grades.

Carcinoma, Ductal, Breast↗
PubMed1994

Decrease of complexity in EEG as a symptom of depression.

Nonlinear dynamic analysis provides new methods for the processing of the electroencephalogram (EEG). We demonstrate here that the EEG dynamics of major depressive subjects is more predictable, that is less complex, than that of control subjects. Moreover, the consequence of treatment upon the EEG dynamics seems to be dependent on the appearance of the illness. Although the specificity of this dynamic signature for different stages of depression is to be confirmed, the assumption of a strong link between a healthy system and a high level of complexity in dynamics is further supported.

Adult↗
PubMed1994

Non-linear forecasting measurements of multichannel EEG dynamics.

This work presents a new method for studying the underlying dynamics of multichannel EEG on the basis of the mathematical theory of dynamical systems. It computes the local loss of predictability and Kolmogorov entropy of the dynamics reconstructed from brain electrical activity. This reconstruction uses multichannel recordings in order to quantify an equivalent of spatio-temporal mapping. Five experimental conditions have been studied: closed eyes at rest, closed eyes and counting even numbers, staring at a spotlight, passive and active auditive odd-ball tasks. The entropy is positive for all the experimental conditions which proves that the underlying EEG dynamics are chaotic. Moreover, on the basis of the dynamical signature it is possible to differentiate 3 types of EEG activity: the rest closed eyes activity, the task closed eyes activity (counting and odd-ball tasks) and the open eyes activity (staring at a spotlight). It is inferred that this index could characterize task-related changes in brain activity.

Adult↗
PubMed1994

Loss of control of pre-motor activation in anxious agitated and impulsive depressives. A clinical and ERP study.

1. Current research uses a variety of traditional validation methods in order to test the clinical expression of biological models in psychiatry. The application of these methods has resulted in a paradoxical situation which requires the definition of new objectives in biological and pharmacoclinical research: the biological specificity of new psychotropic drugs does not assume any congruence between their pharmacological and their therapeutic effects, but raises the question of the relationship between biological systems and clinical symptomatology. The dimensional description of psychopathological disorders may be more appropriate to biological studies in psychiatry. 2. A study was undertaken on a population of twenty-one in-patients fulfilling the DSM III-R criteria for major depressive episode. They were divided into two groups on the basis of contrasting clinical dimensions: anxious-agitation and impulsiveness versus retardation and affective blunting. 3. Significant clinical differences between the two groups on mood profiles were echoed by contrasts in event-related potentials during a go-nogo task: only anxious agitated and impulsive patients developed an abnormal cortical activity, as measured by contingent negative variation (CNV), in the nogo condition. 4. This paper suggests how a paradigm with control of motor action leads to specify premotor activation abnormalities in the agitated impulsive depression subtype.

Adult↗
PubMed1993

Loss of heterozygosity and K-ras gene mutations in gastric cancer.

In order to identify relevant genetic lesions in gastric carcinoma, we searched for tumor suppressor gene inactivation and K-ras gene mutations by analyzing tumor and control DNAs from 34 patients. These were from an epidemiologically defined area of Italy characterized by one of the world's highest incidences of stomach cancer. Allele losses were investigated by the Southern blotting procedure at 16 polymorphic loci on 11 different chromosomes. Our data demonstrate that chromosomal regions 5q, 11p, 17p and 18q are frequently deleted, and that 7q and 13q chromosome arms are also involved, although at a lower frequency. Loss of heterozygosity (LOH) at region 11p was not found during other surveys carried out on patients of different geographic origins. No specific combination of allelic losses could be recognized in the samples analyzed, the only exception being that tumors with 17p allelic loss also showed LOH on the 18q region. When matching frequent LOH events and the stage of progression of the tumors, we observed a trend of association between advanced stages and allelic losses on 17p and 18q chromosome arms. The analysis of K-ras, carried out by the polymerase chain reaction and denaturing gradient gel electrophoresis, demonstrated transforming mutations in only 3 out of 32 cases. Colorectal tumorigenesis proceeds by the accumulation of genetic alterations, including K-ras mutations and inactivation of tumor suppressor genes on the 5q, 17p and 18q regions. Our data indicate that, although gastric and colorectal neoplasias share common genetic alterations, they probably progress through different pathways.

Alleles↗
PubMed1993

Base transitions are the most frequent genetic changes at P53 in gastric cancer.

We searched for P53 mutations in gastric carcinoma by analyzing tumor DNAs from 29 patients. We detected 13 different somatic mutations in 15 patients (52%) and a biallelic polymorphism in exon 6 (5 heterozygous subjects). The somatic mutations were mainly localized in the sequences corresponding to the highly conserved domains of the protein. Twelve samples showed a single base change: 11 missense and 1 nonsense mutations. Three samples showed deletions leading to a frame shift, to the in-frame loss of 2 amino acids, and to the deletion of a splicing site. All point mutations, except one, were transitions, and 91% of them were G:C-->A:T changes. We previously analyzed this panel of tumors for allelic loss at the 17p13 chromosomal region, where the P53 gene had previously been located: the results showed an increasing incidence of allelic loss in late-stage tumors. On the contrary, in the present study no trend between P53 mutations and tumor stages was found. This observation indicates that mutation events precede allelic loss in gastric cancer. Half (54%) of the mutations occurred in samples without allelic loss, suggesting that specific mutated alleles, acting in a dominant negative fashion, can alter in vivo the P53 protein function.

Amino Acid Sequence↗
PubMed1993

A dynamical analysis of oscillatory responses in the optic tectum.

Multi-unit recordings from the optic tectum of an awake pigeon displaying oscillatory behavior evoked by visual stimulus are highly non-stationary and contain a broad band of frequencies under a time-window analysis. Here we extend these observations by a non-linear dynamical analysis of these oscillatory signals (local fields potentials) in successive epochs during background activity and visual responses. Two numerical estimates have been obtained from the original data every 200 ms: (1) correlation dimension and (2) non-linear forecasting of the trajectories. Results from eight different recording sites analyzed are consistent and indicate, in the average, an increase in complexity of the signal during the oscillatory periods.

Animals↗